Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39

In May 1993, an outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States was caused by the previously unrecognized Sin Nombre virus (SNV). Most HPS patients had an influenza-like prodrome, followed by rapid onset of pulmonary edema (fatality rate, 52%). To define the magnitude of the outbreak, patients with milder illnesses who sought medical care in the outbreak area during the outbreak period were assessed for infection with SNV. Of 299 study subjects, 43 had illnesses similar to the HPS prodrome. One laboratory finding, thrombocytopenia, was highly discriminatory between non-HPS patients (1%) and confirmed HPS patients (71%; P < .001) during the prodrome phase. No study subject had serologic evidence (IgM antibodies) of recent SNV infection. Five had IgG titers consistent with a previous hantavirus infection: 3 of these 5 were among the 43 patients who had illnesses similar to the HPS prodrome (P < .05). These data provide evidence that mild illness is rarely caused by SNV.
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PMID:Evaluation of the magnitude of the 1993 hantavirus outbreak in the southwestern United States. 765 65

The fat embolism syndrome is an uncommon clinical disorder that typically occurs as a complication of severe trauma. We report the case of a 60-year-old single-lung transplant recipient who died of massive fat emboli. Before lung transplantation, the patient had been treated with corticosteroids for at least 1 year because of chronic obstructive pulmonary disease caused by centrilobular emphysema and asthmatic bronchitis. After receiving his lung transplant, he was treated with triple-drug immunosuppression, which included 25 mg of prednisone per day. He was discharged from the hospital 2 months after transplantation only to be readmitted 2 weeks later with cytomegalovirus pneumonia, from which he recovered. Concomitantly, he had new lumbar compression fractures with severe back pain and lost approximately 3 cm in height during a 3-week period. On the eleventh day after hospital readmission, he suddenly had a "sepsis-like" illness without a known infectious cause, numerous petechiae and ecchymoses, marked pulmonary edema with worsening diffuse pulmonary infiltrates, profound hypoxemia, decreased mentation, and mild thrombocytopenia. He died 3 days later. With the exception of a positive sputum culture for cytomegalovirus, all cultures were negative. The postmortem examination showed severe osteoporosis, multiple vertebral compression fractures, and widespread massive fat emboli. This is the first reported case of fat emboli as the cause of death in a lung transplant recipient, and the case suggests that the fat embolism syndrome should be considered in the differential diagnosis of a sepsis-like illness in patients who have received steroids during a long period, particularly in the setting of vertebral compression fractures.
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PMID:Fatal fat embolism syndrome after numerous vertebral body compression fractures in a lung transplant recipient. 780 19

In May and June 1993, a handful of previously healthy residents of rural areas in the Four Corners region of the southwestern United States died of acute unexplained respiratory distress, later diagnosed as hantavirus pulmonary syndrome. Their illnesses were characterized most prominently by a prodrome of fever and myalgias, followed by thrombocytopenia, the presence of immature white blood cells on the peripheral smear, and catastrophic respiratory decline associated with the sudden onset of noncardiogenic pulmonary edema and hypotensive shock. Although the primary care doctors who treated these patients were spread over a relatively wide rural geographic area, this cluster was recognized in large part because these patients belonged to a defined cohort receiving medical care from a unified system of interconsulting physicians, the Indian Health Service. By just over 2 weeks after receiving laboratory diagnostic specimens, Public Health Service scientists had identified a newly recognized hantavirus as the cause of this disease cluster and Peromyscus maniculatus (the deer mouse) as the rodent reservoir for this zoonotic virus. The oral history of local American Indian healers describes clusters of similar deaths occurring over three cycles during the twentieth century in association with identifiable ecological markers. The abrupt introduction to Western medical practitioners of a disease long recognized by indigenous healers through illness occurring among a cohort of patients seeking care from medical officers of the U.S. Uniformed Services parallels the initial Western medical recognition of previous human illnesses associated with hantaviral infections through disease outbreaks among military troops. The remarkable speed with which the etiology of this disease was elucidated is attributable to both the power of modern genetic investigational techniques and the scientific groundwork laid by nearly half a century of systematic research on hantaviruses.
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PMID:Etiology and epidemiology of the Four Corners hantavirus outbreak. 786 56

A recent outbreak of a severe pulmonary disease in the southwestern United States was etiologically linked to a previously unrecognized hantavirus. The virus has been isolated from its major reservoir, the deer mouse, Peromyscus maniculatus, and recently named Sin Nombre virus. Clinically, the disease has become known as the hantavirus pulmonary syndrome (HPS). Since May 1993, 44 fatal cases of HPS have been identified through clinicopathological review and immunohistochemical (IHC) testing of tissues from 273 patients who died of an unexplained noncardiogenic pulmonary edema. In 158 cases for which suitable specimens were available, serological testing and/or reverse transcription-polymerase chain reaction (RT-PCR) amplification of extracted RNA was also performed. IHC, serological, and PCR results were concordant for virtually all HPS and non-HPS patients when more than one assay was performed. The prodromal illness of HPS is similar to that of many other viral diseases. Consistent hematological features include thrombocytopenia, hemoconcentration, neutrophilic leukocytosis with a left shift, and reactive lymphocytes. Pulmonary histopathological features were similar in most of the fatal HPS cases (40/44) and consisted of an interstitial pneumonitis with a variable mononuclear cell infiltrate, edema, and focal hyaline membranes. In four cases, however, pulmonary features were significantly different and included diffuse alveolar damage and variable degrees of severe air space disorganization. IHC analysis showed widespread presence of hantaviral antigens in endothelial cells of the microvasculature, particularly in the lung. Hantaviral antigens were also observed within follicular dendritic cells, macrophages, and lymphocytes. Hantaviral inclusions were observed in endothelial cells of lungs by thinsection electron microscopy, and their identity was verified by immunogold labeling. Virus-like particles were seen in pulmonary endothelial cells and macrophages. HPS is a newly recognized, often fatal disease, with a spectrum of microscopic morphological changes, which may be an important cause of severe and fatal illness presenting as adult respiratory distress syndrome.
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PMID:Hantavirus pulmonary syndrome. Pathogenesis of an emerging infectious disease. 788 39

Widespread vaccination has largely eliminated anthrax in Europe (the last case was reported in France in 1972) but the disease remains endemic in many developing countries. The usual cutaneous presentation (malignant pustules) is much more familiar than the various visceral manifestations including digestive tract, pulmonary or meningeal signs. We report a case of a 33-year-old immigrant living in France who was hospitalized for asthenia, dyspnoea, mucopurulant expectoration and moderate diarrhoea 3 days after a 3-month stay in Senegal and Gambia. The temperature was 39 degrees C at admission and blood pressure 110/70 mmHg. Crepitants were heard at the base of the right lung and the rest of the physical examination was normal. Blood was drawn for culture. Laboratory tests and the chest X-ray led to the diagnosis of pneumopathy and a treatment of amoxicillin and clavulanic acid was given with oxygenotherapy. The patient's temperature returned to normal but over the next 48 hours the dyspnoea worsened together with the black diarrhoea. The abdomen was painful. There were no skin lesions. The chest X-ray revealed an extension of the bilateral pulmonary images and bilateral pleural effusion. Laboratory tests revealed thrombopenia (platelet count 38,000/mm3) hyperleukocytosis (WBC 48,000/mm3) and haemolysis (Hb 4 milligrams). The diagnosis was made on the basis of the initial blood cultures which were positive for Bacillus anthracis. All other samples were negative, including HIV serology. Despite adapted antibiotic therapy (penicillin G, 8MU/day, was initiated on day 2), multiple organ failure occurred with septic shock and pulmonary oedema. The patient died in the intensive care unit on day 7. Fatal outcome due to anthrax is described in 25% of the visceral forms but reaches 100% in cases of septicaemia. The haemolysis observed in this case is not mentioned in the classical descriptions of anthrax. When treating septic syndromes in patients who have returned from endemic zones, clinicians should entertain the diagnosis of anthrax since the risk of fatal outcome is increased greatly in case of delayed diagnosis.
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PMID:[Visceral form of human anthrax imported from Africa]. 802 24

Five children with AML were treated with high-doses of Ara-C (2 g/m2) during consolidation. After 17 cycles the toxicity was evaluated. Granulocytopenia (< 0.5 x 10(9)/l) and thrombocytopenia (< 25 x 10(9)/l) were stated after 15/17 and 13/17 cycles respectively. The nadir of bone marrow suppression appeared between day 10 and 14. In one case treatment related death during severe myelosuppression was noted. In individual cases jaundice with elevated activity of aminotransferases, paralytic ileus and pulmonary oedema were observed. All these adverse reactions were reversible. Other toxicities such as nausea/vomiting, stomatitis, diarrhea, infections and drug related fever were transient. No neurologic toxicity was seen. There is a need for developing a new way of the administration of high-dose Ara-C which could substantially reduce toxicity of the drug.
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PMID:[Preliminary evaluation of adverse effects after administration of arabinoside cytosine (Ara-C) in high doses to children with acute myelogenous leukemia]. 820 12

Antiphospholipid antibody syndrome (APS) has been shown to be associated with arterial and venous thromboses, recurrent miscarriages, and thrombocytopenia. We describe 3 cases of adult respiratory distress syndrome (ARDS) in patients with primary APS. The autopsy in one patient revealed no evidence of vasculitis, but extensive small vessel thrombosis of multiple organs including the lungs was seen. No infectious process, connective tissue diseases, or pulmonary edema could be documented and there was no clinical or laboratory evidence of vasculitis in the other 2 patients. The 2 patients who survived responded dramatically to intravenous steroids.
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PMID:Adult respiratory distress syndrome associated with antiphospholipid antibody syndrome. 823 28

The following study was performed to determine the effects of phosphodiesterase IV (PDE-IV) inhibition and its attenuation of tumor necrosis factor (TNF alpha) production in a rat model of the Adult Respiratory Distress Syndrome (ARDS). Rats were either unexposed (n = 8), pretreated orally with vehicle prior to intratracheal saline exposure (n = 11), pretreated with vehicle prior to 7 mg/kg intratracheal endotoxin (LPS) administration (n = 22), or pretreated with 5 or 50 mg/kg rolipram prior to LPS exposure (n = 6 and 7, respectively). Blood was sampled 1 and 3 hr post LPS exposure and assayed for plasma TNF alpha concentrations. Twenty-four hours after LPS exposure, blood was sampled again for hematologic measurements. The rats were then anesthetized and exsanguinated. Bronchoalveolar lavage (BAL) was performed after the lung of each rat was removed and weighed. Rolipram pretreatment was protective against LPS-induced mortality and also resulted in reduced plasma TNF alpha concentrations. LPS induced pulmonary edema, as indicated by wet/dry lung weight ratio (W/D) and total BAL protein content (TP) was attenuated by rolipram pretreatment. LPS-induced alveolar hemorrhage was reduced by rolipram pretreatment, but LPS-induced pulmonary neutrophilia was not. The hemoconcentration induced by LPS was reduced by rolipram, as was the LPS-induced thrombocytopenia. However, LPS-induced changes in circulating leukocyte populations were actually exacerbated by rolipram. LPS-induced alterations in renal and hepatic function, indicated by increased blood urea nitrogen (BUN), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), were inhibited by rolipram.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic intervention in a rat model of ARDS: IV. Phosphodiesterase IV inhibition. 838 94

We recently reported that the combined administration of lipopolysaccharide (LPS) and platelet-activating factor (PAF) in rats, at doses that are completely devoid of any effect when given alone, caused lung injury characterized by neutrophil adhesion to lung capillaries and postcapillary venules, neutrophil accumulation in the lung parenchyma, platelet-fibrin deposits in postcapillary venules, and pulmonary edema. A marked increase in lung myeloperoxidase activity and an elevation of serum tumor necrosis factor-alpha and thromboxane B2, along with leukopenia and thrombocytopenia, were also noticed. The present study aimed to examine whether repeated LPS-PAF stimulus can cause progressive lung injury reminiscent of adult respiratory distress syndrome (ARDS). A second LPS-PAF challenge, 4 h (n = 11) after the original challenge, induced mortality (69% at 24 h, P < 0.01) and some of the pathological changes seen in clinical ARDS, including severe pulmonary edema, alveolar proteinaceous exudates, monocytic infiltration, and a further increase in lung myeloperoxidase activity (700%, P < 0.01). Repeated LPS-PAF dosing also resulted in sustained increased serum tumor necrosis factor-alpha levels (1,610 +/- 470 pg/ml, P < 0.01) and further exacerbation of the leukopenia (-68 +/- 6%, P < 0.01) and thrombocytopenia (-65 +/- 8%, P < 0.01). These data suggest that repeated LPS-PAF actions are sufficient to elicit pathophysiology of ARDS-like lung injury.
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PMID:ARDS-like lung injury produced by endotoxin in platelet-activating factor-primed rats. 851 98


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